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Emerging Roles of SIRT3 in Cardiac Metabolism

Murugasamy, K and Munjal, A and Sundaresan, NR (2022) Emerging Roles of SIRT3 in Cardiac Metabolism. In: Frontiers in Cardiovascular Medicine, 9 .

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Official URL: https://doi.org/10.3389/fcvm.2022.850340

Abstract

The heart is a highly metabolically active organ that predominantly utilizes fatty acids as an energy substrate. The heart also derives some part of its energy by oxidation of other substrates, including glucose, lactose, amino acids and ketones. The critical feature of cardiac pathology is metabolic remodeling and loss of metabolic flexibility. Sirtuin 3 (SIRT3) is one of the seven mammalian sirtuins (SIRT1 to SIRT7), with NAD+ dependent deacetylase activity. SIRT3 is expressed in high levels in healthy hearts but downregulated in the aged or diseased hearts. Experimental evidence shows that increasing SIRT3 levels or activity can ameliorate several cardiac pathologies. The primary deacetylation targets of SIRT3 are mitochondrial proteins, most of which are involved in energy metabolism. Thus, SIRT3 improves cardiac health by modulating cardiac energetics. In this review, we discuss the essential role of SIRT3 in regulating cardiac metabolism in the context of physiology and pathology. Specifically, we summarize the recent advancements that emphasize the critical role of SIRT3 as a master regulator of cardiac metabolism. We also present a comprehensive view of all known activators of SIRT3, and elaborate on their therapeutic potential to ameliorate energetic abnormalities in various cardiac pathologies.

Item Type: Journal Article
Publication: Frontiers in Cardiovascular Medicine
Publisher: Frontiers Media S.A.
Additional Information: The copyright for this article belongs to the Authors.
Keywords: Glycolysis; Heart failure; Metabolism; Mitochondrial oxidation; SIRT3
Department/Centre: Division of Biological Sciences > Microbiology & Cell Biology
Date Deposited: 15 Jul 2022 05:28
Last Modified: 15 Jul 2022 05:28
URI: https://eprints.iisc.ac.in/id/eprint/74429

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